• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.6
• /
• pp.705-714
• /
• 1998

Cerebral blood vessels relax when extracellular $K^+$ concentrations $([K^+])_e$ are elevated moderately $(2{\sim}15$ mM, $K^+-induced$ vasorelaxation). We have therefore studied the underlying mechanism for this $K^+-induced$ vasorelaxation in the isolated middle cerebral arteries (MCAs). The effects of ouabain and $Ba^{2+}\;on\;K^+-induced$ vasorelaxation were examined to determine the role of sodium pump and/or Ba-sensitive process (possibly, inward rectifier K current) in the mechanism. Mulvany myograph was used to study 24 rats, 18 rabbits, and 10 humans MCAs $(216{\pm}3\;{\mu}m,\;347{\pm}7\;{\mu}m,\;and\;597{\pm}39\;{\mu}m$ in diameter when stretched to a tension equivalent to 55 mmHg). High $K^+$ (125 mM) and $PGF_{2{\alpha}}\;(1{\sim}10\;{\mu}M)$ induced concentration-dependent contractions in all 3 species, while histamine $(10{\sim}50\;{\mu}M)$ evoked contraction only in the rabbits and induced relaxation in the rats and humans. Addition of $K^+\;(2{\sim}10\;{\mu}M)$ to the control solution induced vasorelaxations. These effects were inhibited by the pretreatment with both ouabain $(10\;{\mu}M)$ and $Ba^{2+}\;(0.1{\sim}0.3\;mM)$ in the rat, but only with ouabain $(10\;{\mu}M)$ in the rabbit and human. These results suggest that $K^+-induced$ vasorelaxation occurs via the stimulation of electrogenic Na pump in the rabbit and human MCAs, while in the rat MCAs via the activation of both Na pump and Ba-sensitive process.

• Journal of Convergence for Information Technology
• /
• v.10 no.10
• /
• pp.143-149
• /
• 2020

This study tried to observe the ability to inhibit vasocontriction in phloretin - the primary ingredient of apple tree leaves and the Manchurian apricot - through ROCK(Rho-associdated, coiled-coil containing protein kinase) inactivation in rat aortae. A piece of artery that was separated from Sprague-Dawley male rats and retained or damaged the endothelium was suspended in myograph tank with two metal rings, the lower ring fixed to the bottom of the tank, and the upper ring connected to the isotonic force transducer. Interestingly, phloretin inhibited fluoride- or phorbol ester-provoked contraction implying that additional pathways dissimilar from endothelial nitric oxide synthesis such as ROCK or MEK (mitogen activated protein kinase kinase) inactivation might be involved in the vasorelaxation. Therefore, this study provides that phloretin participates in the reduction of ROCK or MEK activity in smooth muscle in addition to the endothelial-dependent action of the endotheliuim in complete blood vessels, and consequently inhibits actin-myosin interaction in smooth muscle. Furthermore, phloretin inhibited thromboxane A2-induced contraction suggesting the mechanism including inhibition of ROCK and MEK.

• Korean Journal of Veterinary Research
• /
• v.31 no.2
• /
• pp.171-178
• /
• 1991

Effects of catecholamines were investigated on isolated strips of the male cattle oesophageal groove. In the circular muscles of the bottom and longitudinal muscles of the lip. isometric tensions was recorded with isometric myograph in 25ml organ bath. The results were as follows: 1. The muscular activity was different in preparations from the two parts. In the longitudinal muscle from the lip, rhythmic contractions generally occurred. while in the circular muscle from the bottom they were not seen almost. 2. In the circular muscle of the bottom, the increased tone and biphasic contractions were caused by catecholamines. And these contractions were mediated through $\alpha$-excitatory adrenoceptor. Also circular muscle showed minor inhibitory response to catecholamines. And these effects were mediated through $\beta$-inhibitory adrenoceptor. But the circular muscle was more sensitive to the $\alpha$-excitatory effect than $\beta$-inhibitory effect. 3. In logitudinal muslce of the lip. rhythmic contractions were reduced or disappeared by catecholamines(especially propranolol) and these effects were mediated through $\beta$-adrenoceptor.

• The Korean Journal of Physiology and Pharmacology
• /
• v.18 no.5
• /
• pp.377-381
• /
• 2014

Propofol is a widely used anesthetic. Many studies have shown that propofol has direct effects on blood vessels, but the precise mechanism is not fully understood. Secondary intrapulmonary artery rings from male rats were prepared and mounted in a Multi Myograph System. The following constrictors were used to induce contractions in isolated artery rings: high $K^+$ solution (60 mmol/L); U46619 solution (100 nmol/L); 5-hydroxytryptamine (5-HT; $3{\mu}mol/L$); or phenylephrine (Phe; $1{\mu}mol/L$). The relaxation effects of propofol were tested on high $K^+$ or U46619 precontracted rings. Propofol also was added to induce relaxation of rings preconstricted by U46619 after pretreatment with the nitric oxide synthase inhibitor $N^G$-nitro-L-arginine methyl ester (L-NAME). The effects of propofol on $Ca^{2+}$ influx via the L-type $Ca^{2+}$ channels were evaluated by examining contraction-dependent responses to $CaCl_2$ in the absence or presence of propofol (10 to $300{\mu}mol/L$). High $K^+$ solution and U46619 induced remarkable contractions of the rings, whereas contractions induced by 5-HT and Phe were weak. Propofol induced dose-dependent relaxation of artery rings precontracted by the high $K^+$ solution. Propofol also induced relaxation of rings precontracted by U46619 in an endothelium-independent way. Propofol at different concentrations significantly inhibited the $Ca^{2+}$-induced contractions of pulmonary rings exposed to high $K^+$-containing and $Ca^{2+}$-free solution in a dose-dependent manner. Propofol relaxed vessels precontracted by the high $K^+$ solution and U46619 in an endothelium-independent way. The mechanism for this effect may involve inhibition of calcium influx through voltage-operated calcium channels (VOCCs) and receptor-operated calcium channels (ROCCs).

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.1
• /
• pp.91-97
• /
• 2017

Hyperglycemia is associated with an increased risk of cardiovascular diseases. It has been demonstrated that chronic exposure to high glucose impaired endothelial functions. However, specific effects of short-term exposure to high glucose on vascular reactivity are controversial. Moreover, the combined effects of other metabolic substrates such as free fatty acids (FFA) on vascular reactivity remain poorly understood. Here we investigate the effects of short-term exposure to high glucose with or without other metabolic substrates including FFAs termed "nutrition full" (NF) solution, on mesenteric (MA) and deep femoral arteries (DFA) of rats. Arterial ring segments were mounted in a double-wire myograph. Contraction in response to phenylephrine (PhE) was determined in control (5 mM) and high glucose (23 mM, HG) environments over a 30 min period. In both arteries, PhE-inducedvasocontraction was enhanced by pre-incubation of HG solution. A combined incubation with HG and palmitic acid ($100{\mu}M$) induced similar sensitization of PhE-contractions in both arteries. In contrast, high $K^+$-induced contractions were not affected by HG. Interestingly, pre-incubation with NF solution decreased PhE-induced contraction in MA but increased the contraction in DFA. In NF solution, the HG-induced facilitation of PhE-contraction was not observed in MA. Furthermore, the PhE-induced contraction of DFA was attenuated by HG in NF solution. Our results demonstrate that the sensitization of PhE-induced arterial contraction by HG is differentially affected by other metabolic substrates. The conversation of skeletal arterial contractility by HG in NF solution requires careful interpretation of the previous in vitro studies where only glucose is included in physiological salt solutions. Further studies are required to elucidate the mechanism underlying the inconsistent effect of NF solution on MA and DFA.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.3
• /
• pp.321-328
• /
• 1999

Pulmonary blood vessels with diameters of $200{\sim}400\;{\mu}m$ produce considerably more force in response to vasoconstrictor drugs than those which are either smaller or larger. We have therefore investigated whether or not hypoxic pulmonary vasoconstriction (HPV) is more powerful in vessels of these diameters. We have also looked at the possibility that vessels from different regions of the lung respond differently. To do this we have grouped vessels according to their location within the lung as well as by size. We used a small vessel myograph (Cambustion AM10, Cambridge, UK) to study 208 preconstricted $(1\;{\mu}M\;PGF_{2{\alpha}})$ small pulmonary arteries $(300{\sim}800\;{\mu}m$ diameter when stretched to a tension equivalent to 25 mmHg transmural pressure) from 39 rats anaesthetized with 2% inspired halothane. A biphasic contraction was observed in response to hypoxia (ca. 25 mmHg $Po_2).$ The magnitudes of both the first, transient, phase (PT, peak tension) and of the second, sustained, phase (SST, steady state tension) were measured. The latter was measured 40 min after the start of hypoxia. The first phase was most pronounced in vessels with an average diameter of 423 ${\mu}m$ while the second phase was most pronounced in larger vessels (mean diameter 505 ${\mu}m).$ These maximal responses were all seen in vessels somewhat larger than reported by others. The responses of smaller vessels $(400{\sim}500\;{\mu}m)$ did not depend upon their location within the lung, but those of larger vessels $(600{\sim}700\;{\mu}m)$ showed regional differences. Those from the right lobe and those from the base of the lung gave the largest responses. It was especially noticeable that large vessels (631 ${\mu}m$ diameter) from the base of the right lung gave the biggest responses. Thus HPV seems to occur not in a uniform manner, dependent solely to the size of vessels, but it also depends to some degree on the region of the lung from which vessels have been taken. Furthermore, our results suggest that larger vessels, as well as smaller ones, may contribute significantly to HPV.

• The Korean Journal of Physiology and Pharmacology
• /
• v.20 no.5
• /
• pp.441-447
• /
• 2016

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (${\alpha}_2$-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of $10^{-8}{\sim}10^{-6}mol/L$, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or $3{\times}10^{-9}mmol/L$) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial ${\alpha}_2$-adrenoceptor and nitric oxide synthase.

• The Korean Journal of Physiology and Pharmacology
• /
• v.23 no.5
• /
• pp.403-409
• /
• 2019

Free fatty acid (FFA) intake regulates blood pressure and vascular reactivity but its direct effect on contractility of systemic arteries is not well understood. We investigated the effects of saturated fatty acid (SFA, palmitic acid), polyunsaturated fatty acid (PUFA, linoleic acid), and monounsaturated fatty acid (MUFA, oleic acid) on the contractility of isolated mesenteric (MA) and deep femoral arteries (DFA) of Sprague-Dawley rats. Isolated MA and DFA were mounted on a dual wire myograph and phenylephrine (PhE, $1-10{\mu}M$) concentration-dependent contraction was obtained with or without FFAs. Incubation with $100{\mu}M$ of palmitic acid significantly increased PhE-induced contraction in both arteries. In MA, treatment with $100{\mu}M$ of linoleic acid decreased $1{\mu}M$ PhE-induced contraction while increasing the response to higher PhE concentrations. In DFA, linoleic acid slightly decreased PhE-induced contraction while $200{\mu}M$ oleic acid significantly decreased it. In MA, oleic acid reduced contraction at low PhE concentration (1 and $2{\mu}M$) while increasing it at $10{\mu}M$ PhE. Perplexingly, depolarization by 40 mM KCl-induced contraction of MA was commonly enhanced by the three fatty acids. The 40 mM KCl-contraction of DFA was also augmented by linoleic and oleic acids while not affected by palmitic acid. SFA persistently increased alpha-adrenergic contraction of systemic arteries whereas PUFA and MUFA attenuated PhE-induced contraction of skeletal arteries. PUFA and MUFA concentration-dependent dual effects on MA suggest differential mechanisms depending on the types of arteries. Further studies are needed to elucidate underlying mechanisms of the various effects of FFA on systemic arteries.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.6
• /
• pp.695-703
• /
• 1998

$[K^+]_o$ can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of $[K^+]_o$ in the range of $5{\sim}15$ mM may affect tensions of blood vessels and can change their sensitivity to various vasoactive substances. Therefore, it was examined in the present study whether the sensitivity of cerebral arteries to vasoactive substances can be changed with the moderate increase of $[K^+]_o$, using Mulvany-type myograph and $[Ca^{2+}]_c$ measurement. The contractions of basilar artery and branch of middle cerebral artery induced by histamine were not increased with the elevation of $[K^+]_o$ from 6 mM to 9 mM or 12 mM. On the contrary, the contractions induced by serotonin were significantly increased with the elevation of $[K^+]_o$. The contractions were also significantly increased by the treatment with nitro-L-arginine $(10^{-4}$ M for 20 minutes). In the nitro-L-arginine treated arteries, the contractions induced by serotonin were significantly increased with the elevation of $[K^+]_o$ from 6 mM to 12 mM. $K^+-induced$ relaxation was evoked with the stepwise increment of extracellular $K^+$ from 0 or 2 mM to 12 mM by 2 mM in basilar arterial rings, which were contracted by histamine. But $[K^+]_o$ elevation from 4 or 6 mM to 12 mM by the stepwise increment evoked no significant relaxation. Basal tension of basilar artery was increased with $[K^+]_o$ elevation from 6 mM to 12 mM by 2 mM steps or by the treatment with ouabain and the increase of basal tension was blocked by verapamil. The cytosolic free $Ca^{2+}$ level was not increased by the single treatment with serotonin or with the elevation of $[K^+]_o$ from 4 mM to 8 or 12 mM. In contrast to the single treatment, the $Ca^{2+}$ level was increased by the combined treatment with serotonin and the elevation of $[K^+]_o$. The increase of free $Ca^{2+}$ concentration was blocked by the treatment with verapamil. These data suggest that the sensitivity of cerebral artery to serotonin is increased with the moderate increase of $[K^+]_o$ and the increased sensitivity to serotonin is due to the increased $[Ca^{2+}]_i$ induced by extracellular $Ca^{2+}$ influx.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.4
• /
• pp.415-425
• /
• 1999

$[K^+]_o$ can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of $[K^+]_o$ in the range of $5{\sim}15$ mM may affect tensions of blood vessels and cause relaxation of agonist-induced precontracted vascular smooth muscle $(K^+-induced$ relaxation). In this study, effect of the increase in extracellular $K^+$ concentration on the agonist-induced contractions of various arteries including resistant arteries of rabbit was examined, using home-made Mulvany-type myograph. Extracellular $K^+$ was increased in three different ways; from initial 1 to 3 mM, from initial 3 to 6 mM, or from initial 6 to 12 mM. In superior mesenteric arteries, the relaxation induced by extracellular $K^+$ elevation from initial 6 to 12 mM was the most prominent among the relaxations induced by the elevations in three different ways. In cerebral arteries, the most prominent relaxation was produced by the elevation of extracellular $K^+$ from initial 1 to 3 mM and a slight relaxation was provoked by the elevation from initial 6 to 12 mM. In superior mesenteric arteries, $K^+-induced$ relaxation by the elevation from initial 6 to 12 mM was blocked by $Ba^{2+}\;(30\;{\mu}M)$ and the relaxation by the elevation from 1 to 3 mM or from 3 to 6 mM was not blocked by $Ba^{2+}.$ In cerebral arteries, however, $K^+-induced$ relaxation by the elevation from initial 3 to 6 mM was blocked by $Ba^{2+},$ whereas the relaxation by the elevation from 1 to 3 mM was not blocked by $Ba^{2+}.$ Ouabain inhibited all of the relaxations induced by the extracellular $K^+$ elevations in three different ways. In cerebral arteries, when extracellular $K^+$ was increased to 14 mM with 2 or 3 mM increments, almost complete relaxation was induced at 1 or 3 mM of initial $K^+$ concentration and slight relaxation occurred at 6 mM. TEA did not inhibit $Ba^{2+}-sensitive$ relaxation at all and NMMA or endothelial removal did not inhibit $K^+-induced$ relaxation. Most conduit arteries such as aorta, carotid artery, and renal artery were not relaxed by the elevation of extracellular $K^+.$ Among conduit arteries, trunk of superior mesenteric artery and basilar artery were relaxed by the elevations of $[K^+]_o.$ These data suggest that $K^+-induced$ relaxation has two independent components, $Ba^{2+}-sensitive$ and $Ba^{2+}-insensitive$ one and there are different mechanisms for $K^+-induced$ relaxation in various arteries.